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Am J Vet Res. 2005 Nov;66(11):1877-80.

Effects of induction of capacitative calcium entry on equine laminar microvessels.

Author information

1
Department of Physiology and Pharmacology, Institute of Comparative Medicine, University of Georgia, Athens 30602-7389, USA.

Abstract

OBJECTIVE:

To determine the effects of induction of capacitative Ca2+ entry on tone in equine laminar arteries and veins.

SAMPLE POPULATION:

Laminar arteries and veins from 6 adult mixed-breed horses.

PROCEDURE:

Arteries and veins were isolated and mounted on small vessel myographs for the measurement of isometric tension. Capacitative Ca2+ entry was induced by incubating the vessels with the specific Ca2+-ATPase inhibitor thapsigargin (100nM) in a Ca2+-free physiologic salt solution. Capacitative Ca2+ entry-associated contractile responses were determined by the subsequent addition of 2mM Ca2+ to the solution bathing the vessels; in some experiments, either the voltage-gated Ca2+ blocker diltiazem (10microM) or the putative capacitative Ca2+ entry inhibitor trifluoromethylphenylimidazole (300microM) was added to the bathing solution 15 minutes prior to a second 2mM Ca2+ exposure. The Sr2+ permeability of the capacitative Ca2+ entry pathway in laminar vessels was assessed by exposing the vessels to 4mM Sr2+ after induction of capacitative Ca2+ entry with thapsigargin.

RESULTS:

Induction of capacitative Ca2+ entry elicited robust contractile responses in laminar veins but did not increase tone in laminar arteries. In laminar veins, capacitative Ca2+ entry-induced contractile responses were unaffected by preincubation with diltiazem, attenuated by trifluoromethylphenylimidazole, and were impermeable to Sr+.

CONCLUSIONS AND CLINICAL RELEVANCE:

Results indicated that induction of capacitative Ca2+ entry elicits vasoconstriction in equine laminar veins but not in laminar arteries and should therefore be considered a potential mechanism by which selective venoconstriction occurs in horses during the development of acute laminitis.

PMID:
16334943
[Indexed for MEDLINE]

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